Parkinson's disease (PD) affects 0.1% of the population that is older than 40 years of age (Dawson, T. M. and Dawson, V. L. Science. (2003) 302(5646):819-822). It is a neurodegenerative condition with symptoms of motor dysfunctions (bradykinesia, tremors, and disturbance in balance) accompanied by variable cognitive impairment. These characteristics are attributed to a large reduction in striatal dopamine content and a loss of dopaminergic (DA) neurons in substantia nigra pars compacta (Gauthier, S. and Sourkes, T. L Prog Neuropsychopharmacol Biol Psychiatry. (1982) 6(4-6):595-599). The clinical signs of PD appear after DA neuronal death exceeds a threshold of 70-80% and a loss of striatal nerve terminals that exceed 50-60% (Agid, Y., Lancet. (1991) 337(8753):1321-1324). Investigations of the mechanism of development of PD have indicated that the loss of DA neurons in substantia nigra pars compacta is related to deficits in mitochondrial complex-1 (Jenner, P. and Olanow, C. W. Ann Neurol. (1998) (3 Suppl 1):S72-84; Zhang, Y. et al., Neurobiol Dis. (2000) August; 7(4):240-250; Sherer, T. B. et al., Neuroscientist. (2002) June; 8(3):192-197). A tissue culture model system has been developed that employs the neurotoxin MPP (1 methoyl-4-phenyl-pyridium), (Kaul, S. et al., Eur J Neurosci. (2003) 18(6):1387-1401); the metabolite of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydro-pyridium) that inhibits complex-1 in mitochondria. The model replicates most of the features associated with sporadic PD syndrome. In the N27 dopaminergic cells (Kaul, S. et al., Eur J Neurosci. (2003) 18(6):1387-1401; Anantharam, V. et al., J Neurosci. (2002) 22(5):1738-1751) MPP+ generates reactive oxygen species that promote cytochrome c release and caspase-9 and casepase-3 activation that can lead to apoptosis followed by necrosis and inflammation (Dawson, T. M. and Dawson, V. L. Science. (2003) 302(5646):819-822).